The heart and its tributaries are encased in the thoracic skeleton composed of the manubrium, sternum, clavicles, rib cage, and vertebral bodies. This rigid chassis protects the heart, lungs, and great vessels. Trauma may result from penetrating or blunt mechanisms. The bony structures, interestingly, can also provide unique forms of injuries as they cause deflection of bullets, altering vectors of the original direction of penetration or by secondary fragments. Blunt forces can lead to crushing, traction, or torsion injuries to the heart from deceleration. Penetrating trauma to the great vessels usually leads to immediate exsanguination or, through a pattern of injury similar to blunt trauma including pseudoaneurysm, partial transection with intimal flap, thrombosis, and propagation.
Penetrating cardiac trauma is a highly lethal injury, with relatively few victims surviving long enough to reach the hospital. In a series of 1198 patients with penetrating cardiac injuries in South Africa, only 6% of patients reached the hospital with any signs of life.1
With improvements in organized emergency medical transport systems, up to 45% of those who sustain significant heart injury may reach the emergency department with signs of life. It is somewhat frustrating, however, to note the overall mortality for penetrating trauma has not changed significantly, even in the major trauma centers.2
Blunt cardiac injuries have been reported less frequently than penetrating injuries. The actual incidence of blunt cardiac injury is unknown because of the diverse causes and classifications. Thoracic trauma is responsible for 25% of the deaths from vehicular accidents, of which 10–70% of this subgroup may have been the result of blunt cardiac rupture.3 There continues to be tremendous confusion as the term, “blunt cardiac injury/cardiac contusion” is applied to a wide spectrum of pathology.
Penetrating trauma is a common mechanism for cardiac injury, with the predominant etiologies being from firearms and knives (Table 26-1).4 The location of injury to the heart is associated with the location of injury on the chest wall. Because of an anterior-lateral location, the cardiac chambers at greatest risk for injury are the right and left ventricles. In a review of 711 patients with penetrating cardiac trauma, 54% sustained stab wounds, and 42% had gunshot wounds. The right ventricle was injured in 40% of the cases, the left ventricle in 40%, the right atrium in 24%, and the left atrium in 3%. The overall mortality was 47%. This series noted one-third of cardiac injuries involved multiple cardiac structures.4 More complicated intracardiac injuries involved the coronary arteries, the valvular apparatus, and intracardiac fistulas (such as ventricular septal defects). Only 2% of patients surviving the initial injury required reoperation for a residual defect. The majority of these repairs were performed on a semielective basis.4 Thus, the majority of injuries are to the myocardium, and are readily managed by the general/trauma or acute care surgeon.
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Intrapericardial and intracardiac foreign bodies can sometimes cause complications of acute suppurative pericarditis, chronic constrictive pericarditis, foreign body reaction, and hemopericardium.5 Needles and other foreign bodies have been noted after deliberate insertion by patients with psychiatric diagnoses. A report by LeMaire5 recommended removal of intrapericardial foreign bodies that are greater than 1cm in size, that are contaminated, or that produce symptoms.
Intracardiac missiles can be embedded in the myocardium, retained in the trabeculations of the endocardial surface, or free in a cardiac chamber. These result from direct penetrating thoracic injury or injury to a peripheral venous structure with embolization to the heart. Observation might be considered when the missile is small, right sided, embedded completely in the wall, contained within a fibrous covering, not contaminated, and producing no symptoms. Right-sided missiles can embolize to the pulmonary artery, where they can be removed with catheter based techniques, if large. In rare cases, they can embolize through a patent foramen ovale or atrial septal defect. Left-sided missiles can manifest as systemic embolization shortly after the initial injury.
Blunt cardiac injury has replaced the term “cardiac contusion” and describes injury ranging from insignificant bruises of the myocardium to cardiac rupture. Pathology can be caused by direct energy transfer to the heart or by a mechanism of compression of the heart between the sternum and the vertebral column. Cardiac rupture during external cardiac massage as part of cardiopulmonary resuscitation (CPR) can occur.
Blunt cardiac injuries can, thus, manifest as a spectrum of septal rupture, free wall rupture, coronary artery thrombosis, cardiac failure, complex and simple dysrhythmias, and rupture of chordae tendineae or papillary muscles. The specific mechanisms include motor vehicle accidents, vehicular-pedestrian accidents, falls, crush injuries, blast/explosion, assaults, and CPR. Blunt injury may be associated with sternal or rib fractures. In one report a fatal cardiac dysrhythmia occurred when the sternum was struck by a baseball, which may be a form of commotio cordis.6
True cardiac rupture carries a significant risk of mortality. The biomechanics of this injury includes (1) direct transmission of increased intrathoracic pressure to the chambers of the heart; (2) a hydraulic effect from a large force applied to the abdominal or extremity veins, causing the force to be transmitted to the right atrium; (3) a decelerating force between fixed and mobile areas, explaining atriocaval tears; (4) a direct force causing myocardial contusion, necrosis, and delayed rupture; and (5) penetration from a broken rib or fractured sternum.7 From autopsy data, blunt cardiac trauma with chamber rupture occurs most often to the left ventricle. In contrast, in patients that arrive alive to the hospital, right atrial disruption is more common. These are seen at the SVC-atrial junction, IVC-atrial junction or the right atrial appendage. Blunt rupture of the cardiac septum occurs most frequently near the apex of the heart. Multiple ruptures as well as disruption of the conduction system have been reported. Injury to only the membranous portion of the septum is the least common blunt VSD. Traumatic rupture of the thoracic aorta is also associated with lethal cardiac rupture in almost 25% of cases.
Pericardial tears secondary to increased intra-abdominal pressure or lateral decelerative forces can occur on either side, usually parallel to the phrenic nerve; to the diaphragmatic surface of the pericardium; and finally to the mediastinum. Cardiac herniation with cardiac dysfunction can occur in conjunction with these tears. The heart may be displaced into either pleural cavity or even into the abdomen depending on the tear. In the circumstance of right pericardial rupture, the heart can become twisted, preventing venous return, leading to the surprising discovery of an “empty” pericardial cavity at resuscitative left anterolateral thoracotomy. With a left-sided cardiac herniation through a pericardial tear, a trapped apex of the heart prevents the heart from returning to the pericardium and the term “strangulated heart” has been applied.8
Unless the heart is returned to its normal position, hypotension and cardiac arrest can occur. One clue to the presence of cardiac herniation in a patient with blunt thoracic injury is sudden loss of pulse when the patient is repositioned, such as when moved or placed on a stretcher.8
Iatrogenic cardiac injury can occur with central venous catheter insertion, cardiac catheterization procedures, endovascular interventions and pericardiocentesis. Cardiac injuries caused by central venous catheter placement usually occur with insertion from either the left subclavian or the left internal jugular vein.9
Perforation causing tamponade has also been reported with a right internal jugular introducer sheath for transjugular intrahepatic portocaval shunts. Insertion of left-sided central lines, especially during dilation of the line tract, can lead to SVC and atrial perforations. Even optimal technique carries a discrete rate of iatrogenic injury secondary to central venous catheterization. Common sites of injury include the superior vena caval–atrial junction and the superior vena cava–innominate vein junction. These small perforations sometimes lead to a compensated cardiac tamponade. Drainage by pericardiocentesis is often unsuccessful, and evacuation via subxiphoid pericardial window or full median sternotomy is sometimes required. At operation, when the pericardium is opened, the site of injury has sometimes sealed and may be difficult to find.
Complications from coronary catheterization including perforation of the coronary arteries, cardiac perforation, and aortic dissection can be catastrophic and require emergency surgical intervention.10
Other iatrogenic potential causes of cardiac injury include external and internal cardiac massage, right ventricular injury during pericardiocentesis, endovascular interventions, transthoracic percutaneous interventions, and during intracardiac injections.11
Cardiac complications after electrical injury include immediate cardiac arrest; acute myocardial necrosis with or without ventricular failure; myocardial ischemia; dysrhythmias; conduction abnormalities; acute hypertension with peripheral vasospasm; and asymptomatic, nonspecific abnormalities evident on an electrocardiogram (ECG). Damage from electrical injury is due to direct effects on the excitable tissues, heat generated from the electrical current, and accompanying associated injuries (eg, falls, explosions, fires).12
Wounds involving the epigastrium and precordium can raise clinical suspicion for cardiac injury. Patients with cardiac injury can present with a clinical spectrum from full cardiac arrest to asymptomatic with normal vital signs. Up to 80% of stab wounds that injure the heart eventually manifest tamponade.
Rapid bleeding into the pericardium favors clotting rather than defibrination. As pericardial fluid accumulates, a decrease in ventricular filling occurs, leading to a decrease in stroke volume. A compensatory rise in catecholamines leads to tachycardia and increased right heart filling pressures.
The limits of right-sided distensibility are reached as the pericardium fills with blood and the septum shifts toward the left side, further compromising left ventricular function. As little as 60–100 mL of blood in the pericardial sac can produce the clinical picture of tamponade.13
The rate of accumulation depends on the location of the wound. Because it has a thicker wall, wounds to the ventricle seal themselves more readily than wounds to the atrium. Patients with freely bleeding injuries to the coronary arteries present with rapid onset of tamponade combined with cardiac ischemia.
The classic findings of Beck’s triad (muffled heart sounds, hypotension, and distended neck veins) are seen in a minority of acute trauma patients. Pulsus paradoxus (a substantial fall in systolic blood pressure during inspiration) and Kussmaul’s sign (increase in jugular venous distention on inspiration) may be present but are also not reliable signs. A more valuable and reproducible sign of pericardial tamponade is narrowing of the pulse pressure. An elevation of the central venous pressure often accompanies overaggressive cyclic hyper-resuscitation with crystalloid solutions, but in such instances, a widening of the pulse pressure occurs.
Gunshot wounds to the heart that have a larger pericardial defect are more frequently associated with hemorrhage than with tamponade. The kinetic energy is greater with firearms, and the wounds to the heart and pericardium are usually more extensive. Thus these patients often present with exsanguination into a pleural cavity.
Clinically significant blunt cardiac injuries include cardiac rupture (ventricular or atrial), septal rupture, valvular dysfunction, coronary thrombosis, and caval avulsion. These injuries manifest as tamponade, hemorrhage, or severe cardiac dysfunction. Septal rupture and valvular dysfunction (leaflet tear, papillary muscle, or chordal rupture) can initially appear without symptoms but later demonstrate the delayed sequela of heart failure.
Blunt cardiac injury can also present as a dysrhythmia, most commonly premature ventricular contractions, the precise mechanism of which is unknown. Ventricular tachycardia, ventricular fibrillation, and supraventricular tachydysrhythmias can also occur. These symptoms usually occur within the first 24–48 hours after injury.
A major difficulty in managing blunt cardiac injury relates to definitions. “Cardiac contusion” is a nonspecific term, which should probably be abandoned. It is best to describe these injuries, as “blunt cardiac trauma with”—followed by the clinical manifestation, such as dysrhythmia, or heart failure.14
Traumatic pericardial rupture is rare, and most patients with pericardial rupture do not survive transport to the hospital due to other associated injuries. The overall mortality of those who are treated at trauma centers with such injury remains as high as 64%.15 An overwhelming majority of these cases are diagnosed either intraoperatively or at autopsy.8 The clinical presentation of pericardial rupture with cardiac herniation can mimic that of pericardial tamponade with low cardiac output due to impaired venous return. When the heart returns to its normal position in the pericardium, venous return resumes. Positional hypotension is the hallmark of cardiac herniation due to pericardial rupture,8 whereas pericardial tamponade is associated with persistent hypotension until the pericardium is decompressed. Therefore, a high index of suspicion is helpful when evaluating polytrauma patients with unexplained positional hypotension.
The diagnosis of heart injury requires a high index of suspicion. On initial presentation to the emergency center, airway, breathing, and circulation under the Advanced Trauma Life Support protocol are evaluated and established.16 Two large-bore intravenous catheters are inserted, and blood is typed and cross-matched. The patient can be examined for Beck’s triad of muffled heart sounds, hypotension, and distended neck veins, as well as for pulsus paradoxus and Kussmaul’s sign. These findings suggest cardiac injury but are present in only 10% of patients with cardiac tamponade. The patient undergoes focused assessment with sonography for trauma (FAST). If the FAST demonstrates pericardial fluid in an unstable patient (systemic blood pressure <90 mm Hg), transfer to the operating room can then occur.
Patients in extremis can require emergency department thoracotomy for resuscitation. The clear indications for emergency department thoracotomy by surgical personnel include the following17:
Salvageable post-injury cardiac arrest (eg, patients who have cardiac arrest with high likelihood of intrathoracic injury, particularly penetrating cardiac wounds)
Severe post-injury hypotension (ie, systolic blood pressure <60 mm Hg) due to cardiac tamponade, cardiac herniation, air embolism, or thoracic hemorrhage
If, after resuscitative thoracotomy, vital signs are regained, the patient is transferred to the operating room for definitive repair.
Chest radiography is nonspecific but can identify hemothorax or pneumothorax. Other potentially indicated examinations include CT scan for trajectory and laparoscopy for diaphragm injury.
In cases of blunt cardiac injury, conduction disturbances can occur. Sinus tachycardia is the most common rhythm disturbance seen. Other common disturbances include T-wave and ST segment changes, sinus bradycardia, first- and second-degree atrioventricular block, right bundle branch block, right bundle branch block with hemiblock, third-degree block, atrial fibrillation, premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Thus, a screening 12-lead ECG can be helpful for evaluation. From the EAST guideline for screening for blunt cardiac injury, obtaining an ECG is a level 1 recommendation.18
Much has been written about the use of cardiac enzyme determinations (CPK/MB) in evaluating blunt cardiac injury. However, no relationship among serum assays and identification and prognosis of injury has been demonstrated with blunt cardiac injury.19 Therefore, cardiac enzyme assays are not helpful unless one is evaluating concomitant coronary artery disease.19 Recent data, however, suggests that a normal ECG and troponin I effectively rule out blunt cardiac injury.20,21
Surgeons are increasingly performing ultrasonography for thoracic trauma. The FAST examination evaluates four anatomic windows for the presence of intra-abdominal or pericardial fluid.22 Ultrasonography in this setting is not intended to reach the precision of studies performed in the radiology or cardiology suite, but is intended to determine the presence of abnormal fluid collections.23 Ultrasonography is safe, portable, and expeditious, and can be repeated, as indicated. If performed by a trained surgeon, the FAST examination has a sensitivity of nearly 100% and a specificity of 97.3%.22 In urban environments with rapid transport times, the initial FAST may be falsely negative and has been abandoned in some centers. In this context, FAST may be useful to repeat in appropriate cases. As the use of FAST evolves and high-speed abdominal CT scans are readily available, the most universally agreed indication for its use is for evaluation for pericardial blood. Limited cardiac ultrasound is being used by intensivists in the ICU to evaluate cardiac function and volume status.
To evaluate more subtle findings of blunt cardiac injury, such as wall motion, or valvular or septal abnormalities in the stable patient, formal transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE) can be obtained. Transthoracic echocardiography can have a limited use in evaluating blunt cardiac trauma because many patients also have significant chest wall injury, thus rendering the test technically difficult to perform due to limited windows.
Its major use is in diagnosing intrapericardial blood and tamponade physiology. In stable patients or intraoperatively, TEE can be used to evaluate blunt cardiac injury. Cardiac septal defects and valvular insufficiency are readily diagnosed with TEE. Ventricular dysfunction can often mimic cardiac tamponade in its clinical presentation. Echocardiography is particularly useful in older patients with preexisting ventricular dysfunction. However, most blunt cardiac injuries identified by echocardiography rarely require acute treatment.
Subxiphoid pericardial window has been performed both in the emergency department and in the operating room with the patient under either general or local anesthesia. In a prospective study, Meyer and coworkers24 compared the subxiphoid pericardial window with echocardiography in cases of penetrating heart injury and reported that the sensitivity and specificity of subxiphoid pericardial window were 100% and 92%, respectively, compared with 56% and 93% with echocardiography.
They suggested that the difference in sensitivity may have been due to the presence of hemothorax, which can be confused with pericardial blood, or due to the fact that the blood had drained into the pleura.24 Although there has been significant controversy in the past with regard to the indication for subxiphoid pericardial window, recent enthusiasm for ultrasonographic evaluation has almost eliminated the role of subxiphoid pericardial window in the evaluation of cardiac trauma. It is almost never needed in the ED.
Pericardiocentesis has had significant historical support, especially years ago when the majority of penetrating cardiac wounds were produced by ice picks and the (surviving) patients arrived several hours and/or days after injury. In such instances, there was a natural triage of the more severe cardiac injuries, and the intrapericardial blood had become defibrinated and was easy to remove. As there are now probably more injuries from pericardiocentesis than diagnoses acutely, many trauma surgeons discourage pericardiocentesis for acute trauma.11 Indications for its use may apply in the case of iatrogenic injury caused by cardiac catheterization, at which time immediate decompression of the tamponade may be lifesaving, or in the setting when a surgeon is not available. As a diagnostic tool it, has been replaced by the FAST examination. Pericardial exploration is sometimes performed via a trans-diaphragmatic route during laparotomy to evaluate the pericardium (Fig. 26-1).
Only a small subset of patients with significant cardiac injury reaches the emergency department, and expeditious transport to an appropriate facility is important to survival.
Transport times of less than 5 minutes and successful endotracheal intubation are positive factors for survival when the patient suffers a pulseless cardiac injury.25
Definitive treatment involves surgical exposure through an anterior thoracotomy (Fig. 26-2) or median sternotomy. The mainstays of treatment are relief of tamponade and hemorrhage control. Reestablishment of an effective rhythm and coronary perfusion is pursued by appropriate resuscitation.
Exposure of the heart is accomplished via a left anterolateral thoracotomy, which allows access to the pericardium and heart and exposure for aortic cross-clamping if necessary. This incision can be extended across the sternum to gain access to the right side of the chest and for better exposure of the right atrium. Manual access to the right hemithorax from the left side of the chest can be achieved via the anterior mediastinum by blunt dissection. This allows rapid evaluation of the right side of the chest for major injuries without transecting the sternum or placing a separate chest tube. Once the left pleural space is entered, the lung can be retracted to allow clamping of the descending thoracic aorta distal to the left subclavian artery. The amount of blood present in the left chest suggests whether hemorrhage or tamponade is the primary issue. The pericardium anterior to the phrenic nerve is opened, injuries are identified, and repair is performed.
In selected cases, particularly for small stab wounds to the precordium, median sternotomy can be used. This allows exposure of the anterior structures of the heart, but limits access to the posterior mediastinal structures and descending thoracic aorta for cross-clamping.
Cardiorrhaphy should be carefully performed. Poor technique can result in enlargement of the lacerations or injury to the coronary arteries. If the initial treating physician is uncomfortable with the suturing technique, digital pressure can be applied until an experienced surgeon arrives. Other techniques that have been described include the use of a Foley balloon catheter or a skin stapler (Fig. 26-3). As cardiorrhaphy in the emergency center carries a 30% incidence of needlestick to the operator, the skin stapler allows vascular control so the repair can be completed in a more controlled setting.26
Injuries adjacent to coronary arteries can be managed by placing the sutures deep to the artery (Fig. 26-4). Mechanical support or cardiopulmonary bypass is very uncommonly required in the acute setting.4
For multiple fragments in stable patients, diagnosis in the past was pursued with radiographs in two projections, fluoroscopy, angiography or echocardiography. Recently, the multidetector CT scan can be used to diagnose and locate these fragments. The full body topogram scan can identify all missiles, and while artifact and scatter can be a limiting factor, the cross-sectional images can be directed to precisely locate the missiles. Trajectories can be ascertained. Treatment of retained missiles is individualized. Removal is recommended for intracardiac missiles that are left sided, larger than 1–2 cm, rough in shape, or that produce symptoms. Although a direct approach, either with or without cardiopulmonary bypass, has been advocated, a large percentage of right-sided foreign bodies can now be removed by endovascular techniques. Alternatively, they can be trapped against the chamber walls, the muscle incised, the missile removed, followed by cardiorrhaphy.
Balloon occlusion of the aorta was first described in the Korean War by Hughes.27 Resuscitative balloon occlusion of the aorta via femoral artery access is being utilized to avoid the need to open the chest to clamp the aorta. It is primarily recommended for hemodynamically unstable patients with pelvic fractures or intra-abdominal injury, placing the balloon just above the common iliac artery take-offs (zone 3) or at the diaphragm (zone 1), respectively.28,29 This technique is less useful for thoracic vascular injuries, as in its current form, the balloon would occlude the aorta distal to potential injuries resulting in increased hemorrhage.
Much debate and discussion has occurred about the clinical relevance of “cardiac contusion.” It is suggested that this diagnosis should be eliminated because it does not affect treatment strategies. The majority of these patients seen are normotensive patients with normal initial ECG and suspected blunt cardiac injury. These cases are managed in observation units, with no expected clinical significance. Patients with an abnormal ECG are admitted for monitoring and treated accordingly. Patients who present in cardiogenic shock are evaluated for a structural injury, which is then addressed.14
The second edition of the EAST guideline for evaluation of blunt cardiac injury recommends ECG and perhaps troponin I, with selective use of echocardiography and monitoring.18
Many factors determine survival in patients with traumatic cardiac injury, including mechanism of injury, location of injury, associated injuries, coronary artery and valvular involvement, presence of tamponade, length of prehospital transport, requirement for resuscitative thoracotomy, and experience of the trauma team. The overall hospital survival rate for patients with penetrating heart injuries that arrive with signs of life ranges from 30 to 90%.
The survival rate for patients with stab wounds is 70–80%, whereas survival after gunshot wounds ranges between 30% and 40%. Cardiac rupture has a worse prognosis than penetrating injuries to the heart, with a survival rate of approximately 20%.
Complex cardiac injuries include coronary artery injury; valvular apparatus injury (annulus, papillary muscles, and chordae tendineae); intracardiac fistulas; and delayed tamponade. These delayed sequelae have been reported to have a broad incidence (4–56%), depending on the definition. Coronary artery injury is a rare injury, occurring in 5–9% of patients with cardiac injuries, with a 69% mortality rate.4 A coronary artery injury is most often controlled by simple ligation, but bypass grafting using a saphenous vein may be required for proximal left anterior descending or right coronary artery injuries (with cardiopulmonary bypass).4 Off-pump bypass can theoretically be used these injuries, in the highly unlikely event that the patient is hemodynamically stable.
Valvular apparatus injury is rare (0.2–9%) and can occur with both blunt and penetrating trauma.4 The aortic valve is most frequently injured, followed by the mitral and tricuspid valves, though most victims of aortic valve injuries likely die at the scene.
These injuries are usually identified postoperatively after the initial cardiorrhaphy and resuscitation have been performed. Timing of repair depends on the patient’s condition.
If severe cardiac dysfunction exists at the time of the initial operation, and valvular injury is identified, immediate valve repair or replacement may be required; otherwise, delayed repair is more commonly advised.4
Intracardiac fistulas include ventricular septal defects, atrial septal defects, and atrioventricular fistulas, with an incidence of 1.9% among cardiac injuries. The management depends on symptoms and degree of cardiac dysfunction, with only a minority of these patients requiring repair.4 These injuries are also usually identified after primary repair is accomplished, and they can be repaired after the patient has recovered from the original and associated injuries.
Echocardiography should be obtained before repair so that specific anatomical sites of injury and operative planning can be accomplished.
Dysrhythmias can occur as a result of blunt injury, ischemia, or electrolyte abnormalities and are addressed according to the injury (Table 26-2). Delayed pericardial tamponade is rare. It can occur as early as 1 hour to days after the injury.
Penetrating cardiac injury Sinus/supraventricular tachycardia ST segment changes associated with ischemia Ventricular tachycardia/fibrillation Blunt cardiac injury Sinus tachycardia ST segment, T wave abnormalities Atrioventricular conduction defects, bradycardia Ventricular tachycardia/fibrillation Electrical injury Sinus tachycardia ST segment, T wave abnormalities Conduction/bundle branch delay Axis deviation Prolonged QT intervals Paroxysmal supraventricular tachycardia Atrial fibrillation Ventricular tachycardia, fibrillation Asystole (lightning strike) |
As discussed above, secondary sequelae in survivors of cardiac trauma include valvular abnormalities and intracardiac fistulas. Early postoperative clinical examination and ECG findings are unreliable. Thus echocardiography is recommended during the initial hospitalization in all patients to identify occult injury and establish a baseline study.4,24,30 Because the incidence of late sequelae can be as high as 56%, follow-up echocardiography 3–4 weeks after injury has been recommended by some.24,30
Injuries to the thoracic great vessels—the aorta and its brachiocephalic branches, the pulmonary arteries and veins, the superior and intrathoracic inferior vena cava, and the innominate and azygos veins—occur following both blunt and penetrating trauma. Exsanguinating hemorrhage, the primary acute manifestation, also occurs in the chronic setting when a post-traumatic pseudoaneurysm ruptures.
The treatment of great vessel injuries was unusual during the World Wars.31 Current knowledge regarding the treatment of injured thoracic great vessels has been derived primarily from experience with civilian injuries.32 Great vessel injuries have been repaired with increasing frequency, a phenomenon that has paralleled the development of techniques for elective surgery of the thoracic aorta and its major branches and improvements in emergency medical services.
A detailed understanding of normal and variant anatomy and structural relationships is important for the surgeon and any one who is a consultant to the surgeon in the evaluation of imaging studies. Venous anomalies occur, with the most common being absence of the left innominate vein and persistent left superior vena cava. Thoracic aortic arch anomalies are relatively common (Table 26-3). Knowledge of such anomalies is essential for both open and catheter-based therapies.
| Common origin of innominate and left carotid arteries (“bovine arch”) |
| Ductus diverticulum |
| Persistent left ductus arteriosus |
| Aberrant takeoff of the right subclavian artery from the descending thoracic aorta |
| Dextroposition of the thoracic aorta |
| Coarctation of the thoracic aorta |
| Origin of left vertebral artery off the aortic arch |
| Pseudocoarction of the thoracic aorta (“kinked aorta”) |
| Double aortic arch |
| Right ductus arteriosus |
| Persistent truncus arteriosus |
| Cervical aortic arch (persistent complete third aortic arch) |
| Absence of the internal carotid artery |
| Cardio-aortic fistula |
More than 90% of thoracic great vessel injuries are due to penetrating trauma: gunshot, fragments, stab wounds, or therapeutic misadventures.32 Iatrogenic lacerations of various thoracic great vessels, including the arch of the aorta, are reported complications of percutaneous central venous catheter placement. The percutaneous placement of “trocar” chest tubes has caused injuries to the intercostal arteries and major pulmonary and mediastinal vessels. This is occurring with increasing frequency with the placement of pigtail chest tubes. Intra-aortic cardiac assist or occlusion balloons can produce injury to the thoracic aorta.
During emergency center resuscitative thoracotomy, the aorta may be injured during clamping if a crushing (nonvascular) clamp is used. Over inflation or migration of the Swan-Ganz balloon has produced iatrogenic injuries to pulmonary artery branches with resultant fatal hemoptysis; therefore, once a linear relationship has been established between the pulmonary artery diastolic pressure and the pulmonary capillary wedge pressure, further “wedging” may be unnecessary. Covered stent grafts are being used for endovascular repairs of vascular injuries. These can cause iatrogenic injury through access, fixation, rupture or occlusion. Self-expanding metal stents have recently produced perforations of the aorta and innominate artery following placement into the esophagus and trachea, respectively.33
The great vessels particularly susceptible to injury from blunt trauma include the innominate artery origin, pulmonary veins, vena cava, ascending aorta, and, most commonly, the descending thoracic aorta.34 Aortic injuries have caused or contributed to 10–15% of deaths following motor vehicle accidents for nearly 50 years. These injuries usually involve the proximal descending aorta (54–65% of cases), but can involve other segments, such as the ascending aorta or transverse aortic arch (10–14%), the mid- or distal descending thoracic aorta (12%) or multiple sites (13–18%). The postulated mechanisms of blunt great vessel injuries include (1) shear forces caused by the relative mobility of a portion of the vessel adjacent to a fixed portion, (2) compression of the vessel between bony structures, and (3) abrupt, profound intraluminal hypertension during the traumatic event. The pericardial attachments of the pulmonary veins and vena cava and the fixation of the descending thoracic aorta at the ligamentum arteriosum and diaphragm enhance their susceptibility to blunt rupture by the first mechanism. At its origin, the innominate artery may be “pinched” between the sternum and the vertebrae during sternal impact and is actually an aortic arch injury.
Blunt aortic injuries may be partial thickness—histologically similar to an intimal tear—but most commonly are full thickness and therefore equivalent to a ruptured aortic aneurysm that is contained by surrounding tissues. The histopathological similarities between aortic injuries and nontraumatic aortic catastrophes suggest that similar therapeutic approaches be employed. Therefore, in hemodynamically stable patients, the concepts of permissive hypovolemia and minimization of arterial pressure impulse (dP/dT)—which are widely accepted in the treatment of aortic dissection and aneurysm rupture—should be considered in patients with blunt aortic injuries.
In opposition to patients with aortic medial disease where the adventitia is the restraining barrier, with blunt injury to the descending thoracic aorta, it is the intact parietal pleura (not the adventitia) that contains the hematoma and prevents a massive hemothorax.
True traumatic aortic dissection, with a longitudinal separation of the media extending along the length of the aorta, is extremely rare.35 The use of the term, “dissection,” in the setting of aortic trauma should be equally rare, being accurate in only a few cases. Similarly, the terms, “aortic transection” and “blunt aortic rupture,” should be used only when describing specific injuries, that is, full thickness lacerations involving either the entire or partial circumference, respectively. The term blunt aortic injury is probably most descriptive.
Increasingly, patients with thoracic great vessel injury have associated head, abdominal, and extremity injury. Often, preexisting medical conditions are present, such as diabetes, hypertension, coronary artery disease, or cirrhosis. These patients are also on a large variety of medications, often aspirin, warfarin, platelet inhibitors or other anticoagulants. These interfere with the clotting mechanism, and adaptations in treatment may need to be made.
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